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Peritonitis - Complete INICET Review

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1. Definition

• Bailey & Love's Short Practice of Surgery, p. 1109

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2. Classification (Most Important for INICET)

A. By Source (Primary vs Secondary vs Tertiary)

B. By Extent

• Localised: Only one area of peritoneum inflamed; involuntary guarding and rebound tenderness in that area
• Diffuse/Generalised: Entire peritoneal cavity involved; "board-like" rigidity; life-threatening
• Harrison's Principles of Internal Medicine 22E, p. 1113

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3. Causes of Peritonitis

Bacterial (most common)

Non-bacterial

• Chemical: Bile peritonitis, barium, pancreatic enzymes (sterile peritonitis)
• Allergic: Starch peritonitis
• Traumatic: Operative handling
• Ischaemic: Strangulated bowel, vascular occlusion
• Endometriosis: Haemorrhage into peritoneal cavity
• Ruptured dermoid cysts: Release keratins - intense granulomatous reaction
• Miscellaneous: Familial Mediterranean fever
• Bailey & Love, p. 1109; Robbins Pathologic Basis of Disease

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4. Organisms Involved

Secondary Peritonitis (polymicrobial)

• Gram-negative: E. coli (most common), Klebsiella
• Gram-positive: Streptococci, Staphylococcus aureus, Enterococci
• Anaerobes: Clostridium perfringens, Bacteroides (rule in secondary; rule out primary)

Primary (Spontaneous) Bacterial Peritonitis (SBP)

• Single organism (key feature!)
• E. coli (most common), Streptococci, Klebsiella, Pneumococci
• Anaerobes are rare - if present, reconsider diagnosis!
• Harrison's 22E, p. 1114; Robbins

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5. Pathogenesis of SBP (INICET Favorite)

1. Altered gut microbiota (Enterobacteriaceae overgrowth)
2. Small intestinal bacterial overgrowth
3. Deficiency in Paneth cell defensins
4. Portal hypertensive enteropathy
5. Bacterial translocation → haematogenous seeding of ascites
6. Defective complement and opsonisation in ascitic fluid (low protein)
7. Reduced PMN phagocytic activity in advanced liver disease

• Harrison's 22E, p. 1113

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6. Pathology / Morphology (Robbins)

• Dense collections of neutrophils + fibrinopurulent debris coating viscera and abdominal wall
• Serous fluid accumulates → becomes suppurative as infection progresses
• Subhepatic and subdiaphragmatic abscesses may form
• Except in tuberculous peritonitis, reaction usually remains superficial (does NOT penetrate gut wall)
• Fibrin plaques cause bowel loops to adhere to each other and to parietes
• Inflamed peritoneum appears: reddened, thickened, velvety texture
• Robbins, Cotran & Kumar Pathologic Basis of Disease

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7. Clinical Features

Localised Peritonitis

• Pain in the affected area (somatic pain from parietal peritoneum)
• Involuntary guarding - reflex abdominal wall contraction
• Rebound tenderness (Blumberg's sign) - pain worsens on releasing hand
• Phrenic/shoulder-tip pain - if subdiaphragmatic (referred to C5 dermatome)
• Pelvic peritonitis - deep tenderness on rectal/vaginal examination

Diffuse (Generalised) Peritonitis

• Acute, severe abdominal pain - worse on movement, coughing, deep respiration
• "Hippocratic facies" - patient gravely ill looking, lies still
• "Board-like rigidity" - entire abdomen hard on palpation
• Scaphoid abdomen - in thin patients (rectus muscle contraction)
• Constitutional: anorexia, malaise, fever, nausea/vomiting
• Absent/reduced bowel sounds (paralytic ileus)
• Vital signs: tachycardia, pyrexia, hypotension (in advanced cases)
• Late: septic shock, SIRS, MODS → loss of consciousness

Signs may be diminished in obese patients or those on immunosuppressive medications - important INICET catch!

• Bailey & Love, p. 1109-1110

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8. Diagnosis

Laboratory

• CBC: leukocytosis (raised WBC)
• CRP/ESR: elevated
• LFTs, RFTs, electrolytes, blood cultures
• Ascitic fluid tap (MOST IMPORTANT for SBP):
  • >250 PMNs/μL = diagnostic for SBP ✓
  • Culture (inoculate 10 mL directly into blood culture bottle - improves yield)
  • Culture before starting antibiotics

Imaging

• Harrison's 22E, p. 1114; Bailey & Love, p. 1110

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9. Treatment

A. Primary (SBP) Treatment

• Cefotaxime 2g q8h IV - first line (3rd-gen cephalosporin), covers gram-negative bacilli + gram-positive cocci
• Ceftriaxone 2g q24h IV - alternative
• Piperacillin/tazobactam 3.375g q6h IV - broad spectrum option
• Vancomycin - for prior MRSA infection/colonisation
• No need to cover anaerobes in SBP!
• Duration: minimum 5 days if rapid improvement + blood cultures negative; up to 2 weeks if bacteremia or slow improvement

• 1.5 g/kg IV within 6 hours of detection
• 1.0 g/kg IV on day 3
• Greatest benefit when: creatinine ≥1 mg/dL, BUN ≥30 mg/dL, or total bilirubin ≥5 mg/dL
• Reduces risk of hepatorenal syndrome and mortality

• Norfloxacin (long-term prophylaxis in high-risk cirrhotic patients)
• However, overuse → increased ESBL-producing organisms

B. Secondary Peritonitis Treatment (Surgical)

1. Fluid and electrolyte correction
2. Nasogastric tube insertion
3. Urinary catheter
4. Broad-spectrum antibiotics
5. Analgesia
6. Vital system support (ICU if needed)

1. Source control - remove/exclude cause (close perforation, resect gangrenous bowel)
2. Peritoneal lavage ± drainage
3. Time is critical - expedient surgical intervention saves lives

• Must cover gram-negative aerobes + anaerobes (Bacteroides fragilis)
• Options: beta-lactam/beta-lactamase inhibitor combinations, carbapenems
• Duration: 4-5 days with adequate source control
• Most failures = failure to achieve source control / drain abscess
• Harrison's 22E, p. 1114-1116; Bailey & Love, p. 1110

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10. Special Types (INICET MCQ Favorites)

Tuberculous Peritonitis

• Reaction penetrates deeply (unlike other peritonitis)
• Ascites, fever, weight loss, night sweats
• Laparoscopy with biopsy for diagnosis

Bile Peritonitis

• Chemical/sterile peritonitis initially
• Very irritating; usually complicated by bacterial superinfection
• From biliary system perforation/rupture

Starch Peritonitis

• Granulomatous reaction to surgical glove starch
• Type of foreign body peritonitis

Spontaneous Bacterial Peritonitis vs Secondary Peritonitis - Key Differentiator

Familial Mediterranean Fever

• Genetic cause of recurrent peritonitis episodes
• Autosomal recessive; mutation in MEFV gene (pyrin protein)

CAPD-associated Peritonitis

• From peritoneal dialysis catheter contamination
• Staphylococcus epidermidis, S. aureus common

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11. Prognosis

• SBP: In-hospital mortality ~17.6%; 30-day mortality ~23% at tertiary centers
• Reflects advanced underlying liver disease
• Diffuse secondary peritonitis: Life-threatening; MODS/septic shock if not treated urgently
• Intraabdominal abscess: Treatment failure most often = failure to drain

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12. Key INICET Points Summary

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• Harrison's Principles of Internal Medicine 22E (2025), Chapter 137
• Bailey and Love's Short Practice of Surgery 28th Edition, Chapter 65
• Robbins, Cotran & Kumar Pathologic Basis of Disease
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease, Chapter 39
• Goldman-Cecil Medicine International Edition